Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A significant association has previously been found between a betazole-induced decrease in serum group I pepsinogen (PG I) levels and a low peak acid output (PAO) in symptomatic patients with vagotomy and gastric resection or a drainage procedure. This study compares the effect of betazole on serum PG I levels and gastric acid output in 245 unoperated patients (115 duodenal ulcer, 25 prepyloric ulcer, 32 gastric ulcer, 73 nonulcer) and in 73 symptomatic postoperative patients (15 subtotal gastric resection, 28 vagotomy and gastric resection, 30 vagotomy and drainage). A negative serum PGI response (2-hr serum PG I level less than 92% of basal) occurred in 10 (4.1% of the unoperated patients and in 31 (42.5%) of the postoperative patients. Seven (70%) of the former and 29 (93.5%) of the latter patients had a PAO of less than 10 mEq per hr, indicating that a negative serum PG I response is associated with a low PAO in both unoperated and postoperative patients. The PAO was greater than 10 mEq per hr in 93.1% of the 277 patients with a 2-hr serum PG I level of more than 92% of basal. Additional studies revealed that neither aspiration of gastric juice nor perfusion of the stomach with acid altered the serum PG I response. This suggests that topical acid does not modulate the effect of betazole on serum PG I levels. Finally, a negative serum PG I response has been shown to be paradoxical, in that gastric pepsin levels have been found to increase over basal concurrently with the decrease in serum PG I levels.
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PMID:Effect of betazole on serum group I pepsinogen levels: relationship to gastric acid output in unoperated and postoperative patients. 84 14

Serum group I pepsinogen (PG I) levels have been determined by radioimmunoassay in 924 subjects. The mean levels in 300 healthy control subjects and in 389 hospitalized controls were 110.6 and 100.0 ng per ml, respectively. The "normal" range is estimated to be between 50 and 175 ng per ml. The mean level of serum PG I in 7 patients with Zollinger-Ellison syndrome was 503.9 ng per ml; values ranged between 315 and 921 ng per ml. The 77 patients with duodenal ulcer had a mean serum PG I level of 221.3 ng per ml; 49 (63.6%) had values greater than 175 ng per ml. The distribution of serum PG I values was bimodal in the patients with duodenal ulcer whereas it was unimodal in both groups of control subjects. Mean serum PG I levels in 13 patients with both duodenal and gastric ulcer and in 18 patients with prepyloric ulcer were, respectively, 177.2 and 179.4 ng per ml. Approximately one-half of these patients had high values. The 28 patients with gastric ulcer had a mean serum PG I level of 116.6 ng per ml; 6 (21.4%) had high values. With the exception of 3 patients with gastric ulcer, none of the 136 patients with peptic ulcer had a low (less than 50 ng per ml) level of serum PG I. In 37 patients with chronic alcoholism the mean level of serum PG I was 73.4 ng per ml. The observed gradient in the mean level of serum PG I among the groups of patients studied is similar to that which has been reported for maximally stimulated gastric acid output. This finding suggests that the secretory potential of the fundic gland mucosa of the stomach may be reflected by the level of PG I in serum.
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PMID:Serum group I pepsinogens by radioimmunoassay in control subjects and patients with peptic ulcer. 115 38

Serum group I pepsinogen (PG I) levels, basal acid output, and peak acid output (PAO) have been determined in 120 patients, 54 with duodenal ulcer, 14 with prepyloric ulcer, 12 with gastric ulcer, and 40 without ulcer. The correlation between serum PG I and PAO was statistically significant (r = 0.736, P less than 0.001) up to a serum PG I level of 250 ng per ml. Serum PG I levels above 250 ng per ml were associated with a plateau in the PAO. Each of 8 patients with a serum PG I of less than 40 ng per ml had a PAO of less than 10 mEq per hr. Of 34 patients with a serum PG I over 200 ng per ml, 29 (85.3%) had a PAO of greater than 40 mEq per hr and all had a PAO above 34 mEq per hr. Of 51 patients with a serum PG I between 60 and 150 ng per ml, 47 (92.2%) had a PAO of between 10 and 40 mEq per hr. The results indicate that a significant relationship exists between the concentration of PG I in serum and the acid secretory capacity of the gastric mucosa.
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PMID:A study of the relationship between serum group I pepsinogen levels and gastric acid secretion. 119 20

The aim of this experience has been to evaluate the chief cell mass and serum pepsinogen I in gastric ulcer patients. Comparisons were also made with parietal cell mass and acid secretion. Chief cell mass and serum pepsinogen I are not only influenced by the localization of ulcer but, also, by the histological condition of fundic mucosa. In fact, the behaviour of serum pepsinogen I and chief cell mass in type I gastric ulcer is the same observed in case of fundic chronic gastritis without gastric ulcer. In case of gastric ulcer type I with superficial fundic gastritis it emerges normozymogenism with hyperpepsinogenemia++ I, with preatrophic fundic gastritis hypozymogenism with normopepsinogenemia, with atrophic fundic gastritis hypozymogenism with hypopepsinogenemia I. In type II and III gastric ulcer the chief cell mass and serum pepsinogen I behaviour as they do in duodenal ulcer with hyperpepsinogenemia although hypozymogenism is present.
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PMID:[Chief cell mass in gastric ulcer: cyto-secretory correlations]. 139 Nov 49

We have developed enzyme-linked immunosorbent assay (ELISA) for pepsinogen group I and II (PG I.II) in human serum, and clinical significance of serum pepsinogen measurement was evaluated. Serum PG I.II levels in patients with gastric and duodenal ulcer were higher than those in normal healthy subjects. On the other hand, serum PG I levels in patients with pernicious anemia were significantly low levels. In both gastric ulcer and duodenal ulcer, serum PG I.II levels at active stage were higher than healing stage. These results suggested that the measurement of PG I.II levels was useful for screening or monitoring test for the injury of gastric and duodenal mucosa.
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PMID:[Clinical significance of the measurement of serum pepsinogen group I and II by enzyme-linked immunosorbent assay]. 143 35

To examine the relation between gastric ulcer (GU) location and serum pepsinogen I (PGI) level, we measured this marker in 284 endoscopically proved GU patients. Their ulcer locations were further divided according to Johnson's criteria modified to the corpus (type 1a), gastric angle (type 1b), combined with duodenal ulcer (type 2) and prepyloric area (type 3). The number of each subset were 96, 81, 58 and 49, respectively. Mean serum PGI level (99.6 +/- 44.8 ng/ml) of all GU patients showed no difference from that of their sex and age matched controls. Mean serum PGI levels in both type 1a and 1b patients, did not differ from each other but were significantly lower than in controls, in contrast to those in type 2 and 3 patients which were significantly higher than in controls and comparable to the PGI levels of patients with duodenal ulcer. Smoking did not affect mean serum PGI levels in all subsets except the smoking type 2 patients who manifested a significantly higher mean PGI level. Helicobacter pylori infection did not show different serum PGI levels in any subset. In conclusion, different location of ulcer in the stomach results in a characteristic serum PGI level.
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PMID:Serum pepsinogen I levels of gastric ulcer patients are determined by the location of the ulcer crater. 155 52

Serum alpha 1-antitrypsin (A1AT) allo- and phenotypes (including M1, M2 and M3 alleles) were studied in 99 patients with gastric ulcer (GU) and 56 patients with duodenal ulcer (DU) using agarose isoelectric focusing. The results were compared with the A1AT data of a random population sample of similar genetic background (1422 persons). An increase in M2 allotype and M1M2 phenotype as well as a decrease in Z allotype of A1AT was seen in GU in comparison to DU and the random population. There were no particular clinical features which would distinguish patients with M2 allotype from the remainder of the GU group. However, a trend toward elevated serum pepsinogen I and II levels in patients with M2 allotype was seen. When the pepsinogen levels were compared in the GU patient groups with and without M2 allotype, matched between themselves by the state of the gastric mucosa, a statistically significant difference was revealed between pepsinogen II levels in these two groups. No associations were found between DU and any of the A1AT phenotypes.
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PMID:Alpha 1-antitrypsin allo- and phenotypes in gastric and duodenal ulcer. 175 16

Radioimmunoassay was used to determine trypsin, pepsinogen and gastrin content in the blood serum with the use of kits produced by the firm "Oris" (France). A total of 43 patients with peptic ulcer (25 with duodenal ulcer and 18 with gastric ulcer), 20 patients with chronic gastritis and 10 normal subjects were investigated. The study was conducted on an empty stomach and after a test breakfast consisting of 2 boiled eggs, 100 g of cheese, 100 g of white bread, 25 g of butter, 50 g of sugar and 200 g of tea (57 g of proteins, 63 g of fats, 103 g of carbohydrates; calorie value comprised 1212 kcal). It has been shown that food intake is a regulator of gastrin, pepsinogen and trypsin production that permits evaluating functional possibilities of gastrin-producing cells, the main gastric cells and acinar cells of the pancreas. The investigation conducted has evidenced that compensatory shifts in the levels of gastrin, pepsinogen and trypsin taking place in gastroduodenal disease are directed to the improvement of digestive processes.
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PMID:[The effect of food intake on the content of proteolytic enzymes and gastrin in the blood of patients with peptic ulcer and chronic atrophic gastritis]. 179 41

The preparation KG-62 related to iodomethylates of hydroxyalkyl phosphinic acids with muscarinolytic effect has been studied. The study provides data on the development of experimental gastric ulcer among rats after injections of the preparation. On the basis of morphologic, morphometric and biochemical data it has been stated that the preparation KG-62 in a 5 mg/kg dose has a more strong effect leading to quick gastric ulcer healing. It was supposed that not only suppressing action on hydrochloric acid and pepsinogen secretion lies in the mechanism of the effect but also the activation of physiologic regulation in intact tissue.
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PMID:[Use of a new M-cholinolytic drug KG-62 for correction of the course of experimental stomach ulcer]. 179 42

Little is known about the source and spread of Helicobacter pylori, but transmission from infected family contacts has been suggested. We have therefore investigated 15 children with peptic ulcer and their first-degree relatives for H. pylori. Serum anti-H. pylori IgG, pepsinogen I, and gastrin levels were measured. Endoscopy was carried out on the children and relatives, and biopsies were taken from the gastric antrum for histology, microbiology, and urease testing. Six of 11 children with duodenal ulcer (55%) and two of four children with gastric ulcer (50%) were positive for H. pylori. Fourteen of 16 parents (87%) and eight of 13 siblings (61%) of H. pylori-positive children with peptic ulcer were also infected compared with eight of 14 parents (57%) and none of four siblings of H. pylori-negative children with peptic ulcer (P less than 0.10, greater than 0.05, and NS, respectively). The children with H. pylori-negative peptic ulcer and negative siblings combined were younger than positive children with peptic ulcer and positive siblings (P less than 0.001). The reliability of serum anti-H. pylori IgG level as a screening test for infection was confirmed. These findings call into question a pathogenetic role for H. pylori in some childhood peptic ulceration, but do suggest that person-to-person spread of infection occurs.
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PMID:Helicobacter pylori in children with peptic ulcer and their families. 202 57


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